The development of adrenergic nerves and the beta-adrenergic mechanism activated by sympathetic neurotransmitter is studied in the embryonic chick heart. The release of 3H-norepinephrine by chemical and electrical stimuli is used as a measure of transmiter secretion at different stages of development. The effect of released transmitter on cardiac muscle contractility is also used to measure neuroscretion. Reserpine, an antithypertensive drug that interferes with the vesicular storage of norepinephrine in adrenergic nerves, will be used to delay the development of these nerves in embryonic cardiac muscle. In this way, we can determine the relationship between the onset of nerve secretion and "subsentitivity" of receptors to the adrenergic transmitter. The role of acetylcholine-dependent inhibition of beta-adrenergic sympathetic stimulation of heart muscle cells will also be studied. Cyclic AMP seems to be a critical component in the muscarinic inhibition of B-adrenergic stimulation of the avian heart. Experiments will be done with phosphodiesterase inhibitors that prevent metabolic degradation of cyclic AMP. There is some evidence for muscarinic inhibition that depends upon blocking a cyclic AMP-dependent process (calcium permeability and contractions) without changing the concentration of cyclic AMP.